International Journal of Veterinary Science & Technology Review Article Hypersensitivity Reaction: Review - Shimels Tikuye Yalew* Animal Biotechnology Research Program, National Agricultural Biotechnology Research Centre, Ethiopian Institute of Agricultural Research, Holetta, Ethiopia *Address for Correspondence: Shimels Tikuye Yalew, Animal Biotechnology Research Program, National Agricultural Biotechnology Research Centre, Ethiopian Institute of Agricultural Research, Holetta, Ethiopia, Tel: + 251- 913-796-389; E-mail: [email protected] Submitted: 05 August 2020; Approved: 11 August 2020; Published: 13 August 2020 Cite this article: Yalew ST. Hypersensitivity Reaction: Review. Int J Vet Sci Technol. 2020;4(1): 028-032. Copyright: © 2020 Yalew ST. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ISSN: 2640-4397 International Journal of Veterinary Science & Technology ISSN: 2640-4397 Summary Hypersensitivity is an adaptive immune response which occurs in an inappropriate or exaggerated way, resulting in tissue damage or some other detrimental response in the host. There are four types of hypersensitivities those are types I, II and III are antibody mediated and type IV is cell mediated. Type I hypersensitivity (immediate hypersensitivity) involves the production of allergen specifi c IgE which binds to mast cells and causes their degranulation. Type II hypersensitivity reaction involves antibodies of class IgM & IgG, and results in the damage or destruction of cells or tissues. Type III hypersensitivity is mediated by the deposition of immune complexes in blood vessels and tissues. Type IV hypersensitivity is mediated by T cells and macrophages (and their cytokines). Minimizing exposure to potential antigens reactions may decrease the developing of the diseases. Keywords: Hypersensitivity; Type I hypersensitivity; Type II hypersensitivity; Type III hypersensitivity; Type IV hypersensitivity ABBREVIATIONS Type IV hypersensitivity or Delayed hypersensitivity was originally characterized by its time course in which the reactions took ADCC: Antibody Dependent Cell mediated Cytotoxicity; Ag-ab 12-24 hours to develop and persisted for 2-3 days. Th e best known complex: Antigen Antibody Complex; DNFB: Dinitrofl uorobenzene; examples are reactions induced by injecting tuberculin protein into DTH: Delayed type hypersensitivity; ELISA: Enzyme Linked the skin of animals infected by Mycobacterium tuberculosis. Delayed Immunosorbent Assay; IgE: Immunoglobulin E; IgG: hypersensitivity is dependent on the direct action of T cells which Immunoglobulin G; IgM: Immunoglobulin M; MHC: Major recognize antigen aft er it has been processed by antigen-presenting Histocompatibility Complex; RBC: Red Blood Cell; Rh-: Rhesus cells and presented as peptide fragments bound to the Major negative; Rh+: Rhesus positive Histocompatibility Complex (MHC) molecules [6]. INTRODUCTION Th erefore the objective of this review is to make an overview and Hypersensitivity refers to excessive, undesirable (damaging, to give brief notes on types of hypersensitivity. discomfort-producing and sometimes fatal) reactions produced by the normal immune system. Hypersensitivity reactions require a DEFINITION pre- sensitized (immune) state of the host. Immune response recruits Hypersensitivity is an immunological state in which the immune and mobilizes a series of eff ector molecules that induce a localized system “over-reacts” to foreign antigen such that the immune infl ammatory response, which ultimately removes the antigen [1]. response itself is more harmful than the antigen [7]. Th is infl ammatory response usually does not extensively damage TYPE I HYPERSENSITIVITY the host tissues. But under certain conditions, the infl ammatory response produces deleterious eff ects, resulting in signifi cant It is also known as immediate or anaphylactic hypersensitivity. Th e tissue damage or even death; this is termed as hypersensitivity. reaction may involve skin (urticaria and eczema), eyes (conjunctivitis), Hypersensitivity reactions can be divided into four types: type I, type nasopharynx (rhinorrhea, rhinitis), bronchopulmonary tissues II, type III and type IV, based on the mechanisms involved and time (asthma) and gastrointestinal tract (gastroenteritis). Th e reaction may taken for the reaction [2]. cause from minor inconvenience to death (Figure 1). Th e reaction takes 15-30 minutes from the time of exposure to the antigen [3]. Type I hypersensitivity is mediated by IgE and the reaction takes 15-30 minutes from the time of exposure to the antigen. Sometimes the Immediate hypersensitivity is mediated by IgE. Th e primary reaction may have a delayed onset. Th e primary cellular component cellular component in this hypersensitivity is mast cell or basophil. in this hypersensitivity is mast cell or basophil. Th e reaction is Th e reaction is amplifi ed and/or modifi ed by platelets, neutrophils amplifi ed and/or modifi ed by platelets, neutrophils and eosinophils. and eosinophils. A biopsy of the reaction site demonstrates mainly Th e mechanism of reaction involves preferential production of mast cells and eosinophils. Th e mechanism of reaction involves IgE, in response to certain antigens, allergens. Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specifi c IgE antibodies against the suspected allergens [3]. Type II hypersensitivity reaction involves antibody mediated destruction of cells. It is also known as cytotoxic reaction. In this hypersensitivity reaction, specifi c antibody (IgG or IgM) bound to cell surface antigen and destroy the cell. When antibody binds to antigen (microorganism or RBC) they form Ag-ab complex. When complement is activated on the surface of cell (RBC) it causes lysis of cell [4]. Type III hypersensitivity reaction is also known as immune complex hypersensitivity. Th e reaction may take 3-10 hours aft er exposure to the antigen. Type III hypersensitivity is associated with responses to soluble antigens that are not combined with host tissues but with antibodies in the blood which can then lead to infl ammatory Figure 1: Diagrammatic representation of type I hypersensitivity reactions [12]. responses [5]. SCIRES Literature - Volume 4 Issue 1 - www.scireslit.com Page -029 International Journal of Veterinary Science & Technology ISSN: 2640-4397 preferential production of IgE, in response to certain antigens, to antigen (microorganism or RBC) they form Ag-ab complex. allergens. IgE has very high affi nity for its receptor on mast cells and Ag-ab complex can activate complement system by three diff erent basophils. Th ese reactions mediated by agents without IgE-allergen mechanism-classical pathway, alternate pathway and lectin pathway. interaction are not hypersensitivity reactions, although they produce Activated complement proceeds in cascade mechanism. When the same symptoms [8]. complement is activated on the surface of cell (RBC) it causes lysis of cell [15]. Diagnostic tests for immediate hypersensitivity include skin (prick and intradermal) tests, measurement of total IgE and specifi c IgE Antibody Dependent Cell Mediated Cytotoxicity (ADCC) is antibodies against the suspected allergens. Total IgE and specifi c IgE when antibody binds with antigen by its Fab portion. However Fc antibodies are measured by a modifi cation of enzyme immunoassay region of antibody has receptor on cytotoxic cells. So, antibody cross (ELISA) [9]. Symptomatic treatment is achieved with antihistamines link target cell (microorganism or RBC) with cytotoxic cells and which block histamine receptors. Chromolyn sodium inhibits mast promote killing. Most cytotoxic cells contain storage of hydrolytic and cell degranulation, probably, by inhibiting Ca++ infl ux [10]. digestive enzymes. Th ese enzymes are released on the surface of target cell (MOs or RB or target cell), killing them. Here antibody itself does Hyposensitization (immunotherapy or desensitization) is another not kill or destroy cell but rather mediate killing by presenting antigen treatment modality which is successful in a number of allergies, to cytotoxic cell. Similarly cytotoxic cell depends upon antibody to particularly to insect venoms and, to some extent, pollens. Th e bind antigen. So this mechanism is known as Antibody dependent mechanism is not clear, but there is a correlation between appearance cell mediated cytotoxicity [16]. of IgG (blocking) antibodies and relief from symptoms. Suppressor T cells that specifi cally inhibit IgE antibodies may play a role [11]. When antigen enters into host body, antibodies are produced. Antibody binds to antigen through Fab region. Fc region of antibody Mechanism of type I hypersensitivity remains free. Phagocytic cells such as Neutrophils, macrophages and Immediate reaction is a quick release of preformed monocytes have receptors that can bind to Fc region of antibody. Th e immunomodulators, known as mast cells degranulation. Th e allergen receptor is known as FcR. In this case antibody molecule directly cross stimulates the induction of cd4+T cells. Th ese T cells secrete cytokines links antigen (Microrganism or RBC or target cell) with phagocytic that cause IgE production by plasma cells. Th e IgE molecule will cells. Th is cross-linkage activates phagocytic cells and increases the bind to Fc receptor on mast cell and basophils